Older adults who experience traumatic injuries have cardiovascular systems and baroreceptors that produce a tempered response to the release of catecholemines needed to increase heart rate and cardiac output when physiologically stressed (Denke, 2020). Many geriatric trauma patients have comorbidities such as CHF, COPD, ESRD, and DM, to name a few, and common treatments such as beta blockers, cardiac glycosides, and pacemakers further limit the body’s reply to injuries. Therefore, vital signs may not be the best indicator of shock or volume status in geriatric trauma patients. Additionally, reduced urine output may occur from preexisting renal insufficiency (rather than poor tissue perfusion from hypovolemia), altered mental status may be caused by dementia, and poor capillary refill time may be the result of peripheral vascular disease (Plummer, 2020). Lactate levels and base deficit can be used as measurements of adequate tissue perfusion and should assist in determining if fluid resuscitation is sufficient among elderly trauma patients (Plummer, 2020). Smaller fluid boluses, with frequent reassessment for signs of fluid overload (crackles in lungs or increased work of breathing) after each bolus, early administration of PRBCs to maintain tissue perfusion, and prompt reversal of anticoagulants are some interventions conducive to successful, safe fluid resuscication and correction of coagulopathies in geriatric trauma patients (Denke, 2020). On the other hand, inadequate fluid resuscitation may prolong periods of hypovolemia and hypoperfusion, thus increasing morbidity and mortality (Plummer, 2020). In general, isotonic crystalloids such as NS are administered in traumatic brain injured patients (and dextrose-containing fluids are avoided) with the goal of achieving normal or slightly higher than normal sodium and osmolality levels to prevent volume from moving out of the intravascular space and exacerbating cerebral edema.
The most recent data supports the administration of only half to one liter of crystalloid fluid in hypotensive trauma patients, even those who are actively bleeding. Acidosis, coagulopathy, and hypothermia (known as the “trauma triad of death”) exacerbates hemorrhage and can lead to trauma-induced coagulopathy (TIC). The use of NS in trauma resuscitation has been shown to exacerbate the first two aspects of this phenomenon (metabolic acidosis and coagulopathy), as well as effect blood concentration (by causing hemodilution) and induce blood vessel dilation, all of which have the potential to worsen patient outcomes (Fisher & Carius, 2018). A damage control resuscitation strategy combats this and is comprised of permissive hypotension, hemostatic resuscitation, and damage control surgery (DCS). Plasma, platelets, and RBCs in a ratio of 1:1:1 as well as the use of antifibrinolytic agents such as tranexamic acid in addition to limiting the use of crystalloids are mainstays of this approach (Fisher & Carius, 2018). Massive transfusion protocol (MTP) should be activated in patients requiring continued resuscitation and started as early as possible to avoid rapid administration of crystalloids and post-injury complications such as organ failure and abdominal compartment syndrome (Fisher & Carius, 2018).